目的 提高对胺碘酮所致肺间质纤维化的认识,提高其诊断及治疗水平.方法 回顾性分析我院1例因误服过量胺碘酮致肺间质纤维化呼吸衰竭病例并进行相关文献复习.结果 患者,男,60岁,因“咳嗽、乏力伴畏寒2d”于2010年11月13日入院,入院前曾因“阵发性室上速”,给予胺碘酮150mg静注2次、300mg静脉滴注,后改为口服600 mg/d,3次/d,后患者未遵医嘱按时减量,至入院时共使用胺碘酮50 d总量30 g.入院时患者呼吸急促,心率快,口唇及甲床发绀,双侧中、下肺部闻及广泛湿哕音及爆裂音.实验室检查示:白细胞11.18×109/L,中性粒细胞0.87,谷丙转氨酶70 U/L,白蛋白26.3 g/L,总蛋白55.9 g/L,C反应蛋白102.50 mg/L,pH值7.441,PO234.80 mm Hg,PCO229 mm Hg,SaO268.9%,肺部CT示双肺呈间质性改变,以右肺尤著.肺功能检查提示:重度混合性通气功能障碍,肺弥散功能重度降低.诊断为胺碘酮所致肺间质纤维化合并感染,呼吸衰竭Ⅰ型.停用胺碘酮,面罩吸氧,先后给予左氧氟沙星、头孢哌酮/舒巴坦、万古霉素、氟康唑以及甲泼尼龙和乙酰半胱氨酸治疗后逐步好转,激素和乙酰半胱氨酸总疗程为7个月,停药后随访7个月,患者活动后无明显胸闷气促,肺CT间质纤维化改变吸收.结论 肺间质纤维化为胺碘酮常见药物不良反应之一.使用胺碘酮前应进行利益/风险评价,长期用药应使用最小有效剂量,定期检测肺功能,以减少和及时发现肺毒性.一旦临床诊断为肺毒性,应及时减量和停药,多数患者停药后可缓解,严重者需使用糖皮质激素治疗.
目的 提高對胺碘酮所緻肺間質纖維化的認識,提高其診斷及治療水平.方法 迴顧性分析我院1例因誤服過量胺碘酮緻肺間質纖維化呼吸衰竭病例併進行相關文獻複習.結果 患者,男,60歲,因“咳嗽、乏力伴畏寒2d”于2010年11月13日入院,入院前曾因“陣髮性室上速”,給予胺碘酮150mg靜註2次、300mg靜脈滴註,後改為口服600 mg/d,3次/d,後患者未遵醫囑按時減量,至入院時共使用胺碘酮50 d總量30 g.入院時患者呼吸急促,心率快,口脣及甲床髮紺,雙側中、下肺部聞及廣汎濕噦音及爆裂音.實驗室檢查示:白細胞11.18×109/L,中性粒細胞0.87,穀丙轉氨酶70 U/L,白蛋白26.3 g/L,總蛋白55.9 g/L,C反應蛋白102.50 mg/L,pH值7.441,PO234.80 mm Hg,PCO229 mm Hg,SaO268.9%,肺部CT示雙肺呈間質性改變,以右肺尤著.肺功能檢查提示:重度混閤性通氣功能障礙,肺瀰散功能重度降低.診斷為胺碘酮所緻肺間質纖維化閤併感染,呼吸衰竭Ⅰ型.停用胺碘酮,麵罩吸氧,先後給予左氧氟沙星、頭孢哌酮/舒巴坦、萬古黴素、氟康唑以及甲潑尼龍和乙酰半胱氨痠治療後逐步好轉,激素和乙酰半胱氨痠總療程為7箇月,停藥後隨訪7箇月,患者活動後無明顯胸悶氣促,肺CT間質纖維化改變吸收.結論 肺間質纖維化為胺碘酮常見藥物不良反應之一.使用胺碘酮前應進行利益/風險評價,長期用藥應使用最小有效劑量,定期檢測肺功能,以減少和及時髮現肺毒性.一旦臨床診斷為肺毒性,應及時減量和停藥,多數患者停藥後可緩解,嚴重者需使用糖皮質激素治療.
목적 제고대알전동소치폐간질섬유화적인식,제고기진단급치료수평.방법 회고성분석아원1례인오복과량알전동치폐간질섬유화호흡쇠갈병례병진행상관문헌복습.결과 환자,남,60세,인“해수、핍력반외한2d”우2010년11월13일입원,입원전증인“진발성실상속”,급여알전동150mg정주2차、300mg정맥적주,후개위구복600 mg/d,3차/d,후환자미준의촉안시감량,지입원시공사용알전동50 d총량30 g.입원시환자호흡급촉,심솔쾌,구진급갑상발감,쌍측중、하폐부문급엄범습홰음급폭렬음.실험실검사시:백세포11.18×109/L,중성립세포0.87,곡병전안매70 U/L,백단백26.3 g/L,총단백55.9 g/L,C반응단백102.50 mg/L,pH치7.441,PO234.80 mm Hg,PCO229 mm Hg,SaO268.9%,폐부CT시쌍폐정간질성개변,이우폐우저.폐공능검사제시:중도혼합성통기공능장애,폐미산공능중도강저.진단위알전동소치폐간질섬유화합병감염,호흡쇠갈Ⅰ형.정용알전동,면조흡양,선후급여좌양불사성、두포고동/서파탄、만고매소、불강서이급갑발니룡화을선반광안산치료후축보호전,격소화을선반광안산총료정위7개월,정약후수방7개월,환자활동후무명현흉민기촉,폐CT간질섬유화개변흡수.결론 폐간질섬유화위알전동상견약물불량반응지일.사용알전동전응진행이익/풍험평개,장기용약응사용최소유효제량,정기검측폐공능,이감소화급시발현폐독성.일단림상진단위폐독성,응급시감량화정약,다수환자정약후가완해,엄중자수사용당피질격소치료.
Objective To intensify the knowledge about amiodarone induced pulmonary interstitial fibrosis,and improve the level of diagnosis and treatment.Methods A retrospective analysis of one case of amiodarone induced pulmonary interstitial fibrosis with literature review was conducted.Results A 60-year-old patient,who received inappropriate high dose of amiodarone (total 30 g) for 50 days due to paroxysmal supraventicuar fachycardia,was admitted to hospital with chief complaint of cough,fatigure and chilly for two days.The symptoms of the patient included short of breath,sychnosphygmia,cyanosis of lip and a nail bed,bilateral moist rales and crackles.Laboratory tests revealed the following levels and values:white blood cell 11.18 × 109/L,neutrophilic granulocyte 0.87,alanine transaminase 70 U/L,albumin 26.3 g/L,total protein 55.9 g/L,C-reactive protein 102.50 mg/L,pH 7.441,PO2 34.80 mm Hg,PCO2 29 mm Hg,SaO268.9 %.CT scan revealed bilateral pulmonary interstitial fibrosis,especially in the right lung.Lung function testing indicated severe mixed ventilation function obstacle and severe decrease in pulmonary diffusion capacity.The diagnosis was amiodarone induced pulmonary interstitial fibrosis with infection and type Ⅰ respiratory failure.After withdrawing the drug,treatments with inhaling oxygen through a face mask,levofloxacin,cefoperazone/sulbactam,vancomycin,fluconazole,corticosteroid and acetylcysteine therapy were implemented,and the results showed clear clinical,functional and radiological improvement.The treatment with corticosteroid and acetylcysteine totally lasted for seven months,and then a seven months follow up was carried out.The results showed the patient had no obvious short of breath after activities,and obvious fibrosis change was not observed in the lung CT images.Conclusions Pulmonary interstitial fibrosis is one of the common adverse reactions of amiodarone.It is recommended that the benefit/risk ratio should be evaluated at the beginning of amiodarone therapy.For long-term treatment,a smallest effective dosage should be used.Regular pulmonary function test is suggested once the patient receives amiodarone therapy.Once amiodarone pulmonary toxicity occurs,the best option is drug discontinuation or dose reduction.Patients with severe pulmonary fibrosis need systemic cortieosteroid therapy.